Chevalier J F, Renier E, Brion S
Encephale. 1980;6(4):381-4.
The administration of diuretics to a 64 year old patient with Parkinsonian disease treated by amantadine, orphenadrine and Modopart and presenting an oedemia of the legs, induced the apparition of myoclonic jerks similar to those observed in a bismuth intoxication. The myoclonic jerks remained after the diuretics were stopped and only disappeared with the suppression of amantadine. It is supposed that diuretics increased the intoxication by amantadine, probably by means of an increase of the reabsorption of basic drugs. Myoclonius may be caused by the central anticholinergic properties of amantadine.
对一名64岁帕金森病患者使用利尿剂,该患者正在接受金刚烷胺、奥芬那君和麦多巴治疗,且出现腿部水肿,结果诱发了类似于铋中毒时观察到的肌阵挛性抽搐。停用利尿剂后肌阵挛性抽搐仍存在,仅在停用金刚烷胺后才消失。推测利尿剂可能通过增加碱性药物的重吸收增强了金刚烷胺的毒性作用。肌阵挛可能是由金刚烷胺的中枢抗胆碱能特性引起的。